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Special Issue "Lipid Emulsion  in Toxicology"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editor

Prof. Dr. Ju-Tae Sohn
E-Mail Website
Guest Editor
Gyeongsang National University College of Medicine, Department of Anesthesiology and Pain Medicine, Jinju 52727, Korea
Interests: anesthetics; vascular pharmacology; lipid emulsion; local anesthetic toxicity; calcium; nitric oxide; smooth muscle contraction

Special Issue Information

Dear Colleague,

Lipid emulsion was initially developed for parenteral nutrition. Lipid emulsion has been widely used for the treatment of local anesthetic systemic toxicity. In addition, these days, lipid emulsion was reported to be effective in alleviating toxicity of nonlocal anesthetic drugs with high lipid solubility. Although lipid emulsion is used to treat intractable cardiovascular collapse induced by toxicity of nonlocal anesthetic drugs (amitriptyline, bupropion, quetiapine, verapamil, and diphenhydramine) with high lipid solubility, many physicians have a tendency to consider only the lipid sink as the underlying mechanism, in which the lipid emulsion absorbs highly lipid soluble drugs from vital organs, leading to a reduction in the offending drug content in vital organs such as the heart. However, many mechanisms other than the lipid sink have been demonstrated to be involved experimentally, including lipid shuttle (enhanced redistribution), inotropic effects, inhibition of nitric oxide production, fatty acid supply, attenuation of mitochondrial dysfunction, and glycogen synthase kinase-3b phosphorylation. For this Special Issue, we welcome all research papers associated with lipid emulsion treatment of systemic toxicity induced by local anesthetics or nonlocal anesthetic drugs, including antidepressants, antipsychotics, calcium channel blockers, and anti-arrhythmic. Such a collection would be helpful in providing insights toward improving lipid emulsion treatment of toxicity caused by local anesthetic or nonlocal anesthetic drugs.

Dr. Ju-Tae Sohn
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • lipid emulsion
  • local anesthetic toxicity
  • nonlocal anesthetic drug toxicity
  • hypotension
  • cardiac arrest
  • seizure
  • cardiac arrhythmia

Published Papers (1 paper)

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Research

Article
Lipid Emulsion Enhances Vasoconstriction Induced by Dexmedetomidine in the Isolated Endothelium-Intact Aorta
Int. J. Mol. Sci. 2021, 22(7), 3309; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073309 - 24 Mar 2021
Viewed by 425
Abstract
This study aimed to examine the effect of lipid emulsion (LE) on the vasoconstriction induced by dexmedetomidine (DMT) in the isolated rat aorta and elucidate the associated cellular mechanism. The effect of LE, NW-nitro-L-arginine methyl ester (L-NAME), and methyl-β-cyclodextrin (MβCD) on [...] Read more.
This study aimed to examine the effect of lipid emulsion (LE) on the vasoconstriction induced by dexmedetomidine (DMT) in the isolated rat aorta and elucidate the associated cellular mechanism. The effect of LE, NW-nitro-L-arginine methyl ester (L-NAME), and methyl-β-cyclodextrin (MβCD) on the DMT-induced contraction was examined. We investigated the effect of LE on the DMT-induced cyclic guanosine monophosphate (cGMP) formation and DMT concentration. The effect of DMT, LE, 4-Amino-3-(4-chlorophenyl)-1-(t-butyl)-1H-pyrazolo[3,4-d]pyrimidine,4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), and rauwolscine on the phosphorylation of endothelial nitric oxide synthase (eNOS), caveolin-1, and Src kinase was examined in the human umbilical vein endothelial cells. L-NAME, MβCD, and LE (1%, standardized mean difference (SMD): 2.517) increased the DMT-induced contraction in the endothelium-intact rat aorta. LE (1%) decreased the DMT (10−6 M) concentration (SMD: −6.795) and DMT-induced cGMP formation (SMD: −2.132). LE (1%) reversed the DMT-induced eNOS (Ser1177 and Thr496) phosphorylation. PP2 inhibited caveolin-1 and eNOS phosphorylation induced by DMT. DMT increased the Src kinase phosphorylation. Thus, LE (1%) enhanced the DMT-induced contraction by inhibition of NO synthesis, which may be caused by the decreased DMT concentration. DMT-induced NO synthesis may be caused by the increased eNOS (Ser1177) phosphorylation and decreased eNOS (Thr495) phosphorylation potentially mediated by Src kinase-induced caveolin-1 phosphorylation. Full article
(This article belongs to the Special Issue Lipid Emulsion  in Toxicology)
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